prevencion infecciones sitio quirúrgico

Tsai and Caterson Patient Safety in Surgery 2014, 8:42http://www.pssjournal.com/content/8/1/42

REVIEW Open Access

Current preventive measures for health-careassociated surgical site infections: a reviewDavid M Tsai and Edward J Caterson*

Abstract

Healthcare-associated infections (HAIs) continue to be a tremendous issue today. It is estimated 1.7 million HAIsoccur per year, and cost the healthcare system up to $45 billion annually. Surgical site infections (SSIs) aloneaccount for 290,000 of total HAIs and approximately 8,000 deaths. In today’s rapidly changing world of medicine, itis ever important to remain cognizant of this matter and its impact both globally and on the individual lives of ourpatients. This review aims to impress upon the reader the unremitting significance of HAIs in the daily practice ofmedicine. Further, we discuss the etiology of HAIs and review successful preventive measures that have beendemonstrated in the literature. In particular, we highlight preoperative, intraoperative, and postoperative interventionsto combat SSIs. Finally, we contend that current systems in place are often insufficient, and emphasize the benefits ofinstitution-wide adoption of multiple preventive interventions. We hope this concise update and review can inspireadditional dialogue for the continuing progress towards improving patient care and patient lives.

Keywords: Nosocomial, Surgical site infections, Health-care associated infections, Hospital-acquired, Preventive measures

IntroductionSince the early beginnings of modern medicine, nosoco-mial infections or healthcare-associated infections (HAIs)have come hand in hand with any progress in medicineand surgery. Without question, we have come a long waysince the days the “good old surgical stink” was lauded.This now gone era was a time when surgeons took pridein their accumulated filth as a mark of their experienceand professional status, and would thus regularly operatewith bloodstained, unwashed garments [1]. Much of theprogress since then is owed to Joseph Lister, an Englishsurgeon who is considered the father of antiseptic surgery.He championed carbolic acid sterilization, hand washing,clean garments and gloves [2]. Later on, the discovery ofpenicillin in 1928 and its mass production in the 1940s in-creasingly tipped the scales in our favor. And for sometime, it seemed like we were on the brink of victory in thewar against HAIs. Yet any sort of celebration was short-lived, for as our antibiotics became stronger and morepervasive, certain strains of bacteria brooded in defianceand soon emerged resistant to our drugs.

* Correspondence: [email protected] of Plastic Surgery, Brigham and Women’s Hospital, Harvard MedicalSchool, 75 Francis Street, 02115 Boston, MA, USA

© 2014 Tsai and Caterson; licensee BioMed CeCreative Commons Attribution License (http:/distribution, and reproduction in any mediumDomain Dedication waiver (http://creativecomarticle, unless otherwise stated.

Further, as the field of medicine advanced, its verylandscape changed—hospitals grew larger, patient livesextended well beyond what was ever thought possible,and the kinds of diseases doctors treated shifted towardsthat of a chronic nature. This came with consequencesthat became apparent too late. The unbridled use of anti-biotics increased the life expectancy of patients withchronic illnesses, but at the cost of harboring resistant mi-croorganisms. Subsequently, these bugs slowly spread be-yond the doors of the hospital until these fugitive strainsbecame part of the normal flora in the community.This is the matter at hand today, and indeed the impli-

cations are enormous, astronomical even, if we fail to re-main vigilant. The Centers for Disease Control (CDC)estimated in 2002 that 1.7 million HAIs occur annuallyand about 1 in 20 hospitalized patients will develop anHAI, of which, 99,000 will result in deaths [3]. In termsof healthcare expenditure, the annual direct cost of HAIsis approximately $28-45 billion [4]. Greater still are thecosts to a patient when a seemingly “run-of-the-mill”medical or surgical procedure unexpectedly turns into afight for his or her life. Such was the case for 34 patientsin Harborview Medical Center in 1980 when a man with35% total-body-surface-area burn was transferred from aburn unit endemic with methicillin-resistant S. aureus.

ntral Ltd. This is an Open Access article distributed under the terms of the/creativecommons.org/licenses/by/4.0), which permits unrestricted use,, provided the original work is properly credited. The Creative Commons Publicmons.org/publicdomain/zero/1.0/) applies to the data made available in this

Tsai and Caterson Patient Safety in Surgery 2014, 8:42 Page 2 of 13http://www.pssjournal.com/content/8/1/42

Even with standard wound precautions, this antibiotic-resistant S. aureus was transmitted to 34 other patients.Ultimately, 27 were infected and 17 of the 34 died [5].At present we live in a world of unparalleled capability

in science, technology, and medicine. Things that wereonce only imagined in fiction and sci-fi movies arequickly becoming our reality. Not only do we routinelyperform heart and lung transplants, but we have enteredthe realm of face and hand transplantation. Despite allthese advances, health-care associated infections have re-peatedly proven to remain a formidable force that loomsin the background—one that if we don’t actively andcontinually combat can threaten to undo any good westrive to accomplish.

DefinitionHealthcare-associated infection is officially defined bythe CDC/National Healthcare Safety Network (NHSN)Surveillance as “a localized or systemic condition result-ing from an adverse reaction to the presence of an infec-tious agent(s) or its toxin(s) [6,7]. There must be noevidence that the infection was present or incubating atthe time of admission to the acute care setting.” The“big four,” which are the 4 most common types, areurinary tract infections (UTI), surgical site infections(SSI), bloodstream infections (BSI), and pneumonia(PNEU) [6,7]. SSIs account for roughly 1/3 of all HAIs,and catheter-associated BSIs, catheter-associated UTIs,and ventilator-associated pneumonias account for theremaining 2/3 [6,7].SSIs are classified into incisional and organ/space, with

specific criteria for each [6,7]. Incisional is sub-classifiedinto superficial incisional, involving only the skin andsubcutaneous tissue, and deep incisional, involving fasciaand muscle. Organ/space SSI involves any part of thebody that was opened or manipulated during the oper-ation, excluding the incision, fascia, and muscle layers.For a more detailed description of each, including signs/symptoms, please refer to CDC/NHSN criteria [6,7].

GoalsThe goal of this review is to impress that this issueshould be paramount to the daily practice of medicine.To that aim, we provide an update and succinct sum-mary of the literature regarding the etiology of HAIs andhighlight some preventive measures that can be success-fully implemented, specifically concerning SSIs. We alsobriefly introduce a novel treatment methodology thatour lab has been developing as a potential avenue tocombat nosocomial SSIs. Lastly, we want to emphasizethe implications of this issue to the healthcare systemand to the individual patient.

Pathophysiology/etiologyThe etiology of HAIs is undeniably multifactorial. How-ever, the source of contamination can often be attributedto the endogenous skin flora of either the patient or hos-pital staff [8-10]. There are two categories of flora: residentand transient [9,11,12]. Resident flora are microorganismsthat normally colonize an individual and live in harmonywith the host, usually providing some benefit or protec-tion [9,11,12]. Conversely, transient flora are microor-ganisms picked up from the environment. They oftendo not survive very long on the host, but are easilytransmissible from one to another or back to the envir-onment [9,11,12].Often referred to as the human “microbiota”, the resi-

dent flora vastly outnumber human host cells by 10–100times and form a commensal community. Over the pastdecade, new sequencing technologies and emerging fieldssuch as metagenomics have enabled researchers to begincharacterizing this intricate, dynamic micro-ecosystemand its implication on host health and disease [12-16]. Itis thought that a disruption or alteration of the complexinteractions among human cells and endogenous microor-ganisms can lead to disease states, such as autoimmune,metabolic, infectious, inflammatory, and even psycho-logical disorders. In the realm of HAIs, studies have sug-gested that the microbiota can act as a physical barrier tocolonization and/or keep the potential virulence of someendogenous microorganisms in check [12-16]. An insultto host homeostasis whether as a consequence of surgeryor another process may in fact disturb the balance of thisdelicate ecosystem, permitting the overgrowth of specificstrains of resident flora with pathogenic potential and/orcolonization of transient flora, transmitted by the environ-ment or by hospital staff [12-16].Some of the most common microorganisms that ac-

count for HAIs include coagulase-negative staphylococci,Staphylococcus aureus, Enteroccocus species, Candida,Escherichia coli, Pseudomonas, and Klebsiella [17]. Thereis a significant percentage of HAIs associated withmultidrug-resistant pathogens (~16%) [17]. The mostcommon includes Methicillin-resistant Staphylococcusaureus (MRSA), accounting for 8%, Vancomycin-resistantEnterococci faecium (VRE), and Carbapenem-resistant P.aeruginosa [17]. About 25-30% of the community isnow colonized by S. aureus and up to 5% are colonizedwith MRSA [18].These microorganisms spread through many routes.

The most common of which includes contact, air, water,and vehicle.• Contact transmission is by direct contact, and per-

haps the most common and easiest way for resident andtransient flora to spread to a susceptible patient. It is alsothe route most easily traced back to healthcare workersand staff. This is often due to improper hand hygiene,


poor antiseptic technique, contaminated needles, instru-ments, or dressings.• Air transmission is often invisible and insidious

since microorganisms carried in the form of airbornedroplets can travel long distances, especially if ventila-tion is poor. Coughing and sneezing are common waysthese pathogens can become airborne. A proper filtra-tion system in place is helpful to prevent hospital-widetransmission.• Water transmission is an underappreciated route

for the spread of pathogens. Contaminated hospital watercan cause devastating nosocomial outbreaks. It is esti-mated that waterborne pseudomonas infections kill 1400annually in the US [19]. Moreover, opportunistic fungi arealso a significant threat, especially to immunocomprom-ised patients [20,21].• Vehicle transmission is by contaminated surfaces

and objects such as food, medications, devices, and equip-ment. This mode, like contact transmission, is often thecause of cross-transmission among susceptible patients,and can easily cause an outbreak. Objects likely to harborviable pathogens are known as fomites and includes com-mon day use objects like stethoscopes, marking pens, ties,and ID lanyards. Studies have shown that stethoscopes arecommonly colonized with S. aureus and MRSA, and thatphysicians have poor stethoscope cleaning practices[22-24]. Contaminated environmental surfaces are alsoan important aspect of this mode of transmission. Path-ogens easily cross-transmit via bed rails, call buttons,trays, chairs, door handles, tabletops, and also throughimproperly cleaned equipment such as ultrasound ma-chines or defibrillators.

Preventive measuresBelow, we have compiled a concise summary of the mostcommon preventive measures in the literature. Peri-operative measures are broken down into preoperative,intraoperative, and postoperative to highlight the manyconsiderations before, during, and after a procedure.This is not meant to be conclusive, but rather, a quickresource from which a dialogue can be sparked regard-ing what more can be done to prevent nosocomial SSIs.For a more comprehensive look into grades of recom-mendations and levels of evidence, please refer to Boscoet al., Savage et al., or Fletcher et al. [25-27].

Hand hygieneImproved hand hygiene is the most important preventivemeasure we can take. Yet compliance is often low. Health-care workers often forget or don’t spend enough timewashing. The CDC recommends washing for at least 20seconds or the duration of the “Happy Birthday” songsung twice [28]. The World Health Organization (WHO)has developed a multimodal approach to improve hand

hygiene compliance. In a study done during a two-yearperiod in Costa Rica, Italy, Mali, Pakistan, and SaudiArabia, they implemented their approach and found thatoverall compliance increased from 51.0% to 67.2% [29].Their strategy consists of five main components: access,training and education, monitoring and feedback, visualreminders, and creation of culture. The WHO details 5key moments hand hygiene should be practiced [30]:

1. Before touching a patient2. Before clean and aseptic procedures3. After contact with bodily fluids4. After touching a patient5. After touching a patient’s surroundings

The question of which method of hand-washing isbetter, traditional hand-scrubbing or hand-rubbing withaqueous alcoholic solution has been studied. The gen-eral consensus is that if your hands are visibly dirty,traditional hand-scrubbing with soap and water is best.Otherwise, hand-rubbing with aqueous alcohol is com-parable [27,31-34]. A randomized equivalence trial com-pared the two and looked at a total of 4387 consecutivepatients who underwent clean and clean-contaminatedsurgery. SSI rates were 55/2252 (2.44%) in hand-rubbingversus 53/2135 (2.48%) in hand-scrubbing [32]. How-ever, compliance was much better in hand-rubbing,presumably due to ease and access, compared to hand-scrubbing (44% vs 28%). There was also better toler-ance, less skin dryness, and irritation [32].

Directed antibiotic therapyWith the increased emergence and threat of multi-drugresistant microorganisms, narrow-spectrum, directed anti-biotic therapy is imperative. Broad-spectrum antibioticsshould be exercised with restraint and only used as aninitial temporizing measure until a specific diagnosis ofthe inciting pathogen is reached. Subsequently, theyshould immediately be discontinued and substitutedwith narrow-spectrum antibiotics. Reduction of broad-spectrum antibiotic use can undoubtedly be curtailedwith the aid of faster, more reliable molecular diagnostictechniques. Next generation methodologies such as PCRsequencing, sonication, and FISH have shown muchpromise, and have been proven superior to traditionalculturing methods in terms of turnover, sensitivity, andaccuracy [35-40]. The continued advancement of thesemolecular tools will revolutionize the way we detect andidentify microorganisms, and ultimately permit rapid,tailored antimicrobial therapy from the very get-go.

Preoperative protocolsThere are several preoperative protocols that show prom-ise in decreasing incidence of HAIs. Some protocols,


however, have little to no benefit, and energy and re-sources should therefore be shifted to those that yield asignificant difference.• Screening for Methicillin-sensitive Staphylococcus

aureus and MRSA:As mentioned, 25-40% of community is colonized with

S. aureus [41-43]. The bacteria usually reside in the an-terior nares. Carriers have been shown to be at higherrisk of staphylococcus infections and are 2-9× as likelyto have SSI [41-43]. They are also at higher risk of noso-comial blood stream infections and lower respiratory in-fections [44-46].In 2002, Perl et al. [47] looked to determine if intranasal

mupirocin reduced rate of S. aureus infections at surgicalsites and prevents other nosocomial infections versusplacebo. In this randomized, double-blind, placebo-controlled trial, they randomly assigned patients, bothcarriers and non-carriers, to either the treatment arm orplacebo arm. Their results indicated that the interven-tion did not significantly decrease rates of S.aureus SSIoverall, but did significantly reduce the rate of nosoco-mial S. aureus among carriers (4.0% vs 7.7%) [47]. Thissuggested the intervention would be more beneficial fornasal carriers rather than an institutional-wide prophy-lactic treatment for all patients.As such, a number of institutions implemented a screen-

ing process followed by decolonization. In one random-ized, double-blind, placebo-controlled multicenter study,rapid identification of carriers by polymerase chain reac-tion followed by treatment with mupirocin nasal ointmentand chlorhexidine soap reduced nosocomial S. aureusinfections. The rate of S. aureus infection was 3.4% (17of 504 patients) in the treatment group versus 7.7% (32of 413 patients) in the placebo group [48]. Similarly, aprospective cohort study of total joint replacement pa-tients demonstrated a decrease in SSI rate in interven-tion patients from 2.7% (20/741) to 1.2% (17/1440) [49].One of the concerns with prophylactic mupirocin ad-

ministration is the development of resistance. In theirstudy, Perl et al. [47] only identified 4 isolates resistant tomupirocin. Three were obtained from those not treatedwith mupirocin. They concluded that a single, short coursedid not appear to select for resistant isolates.• Decolonizing hospital personnel:Following the same principle as preoperative decoloni-

zation of patients, one preliminary study looked at theeffects of decolonizing hospital personnel, specificallythe surgical team [50]. Carriers were identified amongteam members (surgeons, anesthesiologists, nurses) andsubsequently treated with intranasal mupirocin. Retro-spectively, 1000 consecutive patients had yielded 6% SSIrate. Post-intervention, of 300 consecutive patients, therewas a 0% SSI rate [50]. Undoubtedly, more studies areneeded, but this preliminary finding is important since

healthcare personnel are often at fault in the transmis-sion of microorganisms. Institution-wide screening anddecolonization of personnel may be a feasible and suc-cessful preventive measure. At present most hospital sys-tems have no screening methodology for employees withregards to resistant microorganisms. This is in contrast tomandated tuberculosis screening, which overall has a sig-nificantly decreased impact on the healthcare system.• Showering or bathing with skin antiseptics:A Cochrane systematic review investigated the common

practice of preoperative bathing/showering with skin anti-septics as a measure to reduce SSIs. They looked at 7 ran-domized controlled trials with a total of more than 10,000patients that tested chlorhexidine solution against normalsoap or no preoperative washing. They found no evidencesuggesting a clear benefit [51]. Accordingly, it may bewiser to spend effort on more effective interventions.• Antiseptic skin cloths:Another proposed preoperative intervention is the

local application of antiseptic solution at the plannedsurgical site. In a prospective RCT, Murray et al. [52] in-vestigated the efficacy of the home application of a 2%chlorhexidine gluconate (CHG) cloth before shouldersurgery in decreasing the skin surface levels of bacteria.The overall positive culture rate in the treatment groupvs control group was 66% vs 94% (p = 0.0008). The posi-tive culture rate for coagulase-negative Staphyloccocuswas 30% vs 70% (p = 0.0001) [52]. However, there wereno infections in either group, so they were unable to dir-ectly correlate the reduction in culture rates with infec-tion rates. Nevertheless, the culture rates do suggest apotential benefit, especially at the low cost of $3/packageof 2 chorhexidine gluconate cloths [52].In terms of definitive SSI rates, Eiselt [53] demon-

strated its reduction in orthopedic patients undergoingjoint replacements. Patients used a 2% CHG no-rinsecloth the night before the surgery and in the preopera-tive area immediately before the surgery. The controlgroup was historical, prior to the intervention, and in-cluded 727 patients, and the treatment group, prospect-ive, included 736 patients. A significant reduction in SSIrate was demonstrated after the implementation of CHGcloths (3.19% vs. 1.59%) [53].Likewise, Graling et al. [54] conducted a prospective co-

hort study that included 284 patients as a historical con-trol vs 335 patients who received CHG cloth intervention.The overall infection rate was decreased from 6.3% (18/284) to 2.1% (7/335) (p = 0.01). Their economic analysisdiffered slightly from Murray’s. They estimated a total fi-nancial burden of $7 per patient, allotting $2/patient fornursing time for patient education and assistance. This isstill considerable cheaper than the costs associated withpatient morbidity and increased length of stay due to aSSI (estimated at ~ $25,000 per SSI) [55].


• Hair removal:A Cochrane systematic review investigated the routine

practice of preoperative hair removal. They looked todetermine if routine removal compared to no removaland the timing or methods of removal influenced therate of SSIs. 14 trials were included. No statistically sig-nificant evidence was found that indicated hair removalinfluences SSI rate; however, evidence did suggest that ifhair removal was necessary to facilitate surgery or appli-cation of adhesive dressings, clipping compared withshaving reduces the rate of SSIs [56]. Three trials (1343participants) compared the two, and demonstrated signifi-cantly more SSIs associated with shaving than clipping(Relative Risk 2.09, 95% CI 1.15 to 3.80) [56] (Table 1).

Intraoperative protocols• Antibiotics:Prophylactic administration of antibiotics has been

proven effective in reducing the rate of postoperative in-fections for orthopedic, neurological, and spinal surgeries.In a meta-analysis of randomized controlled trials (RCTs)of spine fusion surgery, Baker et al. reported a significantreduction in SSIs, up to 63%, odds ratio 0.37 (95% CI0.17-0.78) [57]. Similarly, other studies have substantiatedthe efficacy of perioperative antibiotics in general orthope-dics, total joint replacement, and spinal surgery [58,59].Several guidelines exist for the prophylactic adminis-

tration of antibiotics. Generally, they advocate a broad-spectrum antibiotic with excellent coverage of S. aureussuch as a first or second-generation cephalosporin (e.g.cefazolin or cefuroxime). For those with beta-lactam aller-gies, clindamycin or vancomycin should be administeredinstead. Moreover, those who are at high risk ofcolonization with MRSA or have had a previous MRSAinfection should be considered for prophylaxis withvancomycin.As for timing and duration, high serum and tissue

levels of antibiotic should be sufficiently obtained priorto the first incision. Therapy should be initiated withinone hour prior to incision, and stopped within 24 hours

Table 1 Summary of preoperative interventions

Preoperative interventions Summary

Screening for MSSA and MRSA ● Screening and prophylactic decS. aureus infections in carriers

Decolonizing hospital personnel ● Preliminary study finds reductiohospital personnel carriers

Showering or bathing with antiseptics ● Cochrane review of 7 RCTs find

Antiseptic skin cloths ● Preoperative application of CHGdecreases skin surface levels of

Hair removal ● Cochrane review finds no evide

● However, clipping, compared t

of closure. Duration greater than 24 hours may lead tosuperinfection with drug-resistant organisms [60]. Forsurgical procedures that are prolonged > 4 hours orincur > 1500 mL of estimated blood loss, a re-dosing isrecommended [61]. Lastly, the compliance of timing,duration, and selection of antibiotics is improved from65% to 99% if the protocol is incorporated into the“time-out” [62].• Skin preparation:Prior to incision, the surgical site is often prepared by

sterilizing the skin. Most commonly, a commercial skinantiseptic solution is applied such as Chloraprep (2%chlorhexidine gluconate and 70% isopropyl alcohol),DuraPrep (0.7% iodine and 74% isopropyl alcohol), orBetadine (0.75% iodine scrub, 1.0% iodine paint). Severalstudies have been conducted to compare the efficacy ofthese common preparation solutions. Ostrander et al. re-ported that ChloraPrep was superior to DuraPrep andTechnicare in terms of eradicating bacteria from theskin, with decreased rates of positive cultures (30% vs.65% vs. 95%, respectively, p < 0.0001) [63]. On the otherhand, Savage et al. found no statistically significantdifference in the rate of positive cultures between Chlor-aPrep and DuraPrep in a prospective study of 100 con-secutive patients undergoing lumbar spinal surgery (0%vs 6%, p = 0.25) [64].As for infection rates, a prospective cohort study that

enrolled 3,209 patients found that DuraPrep was associ-ated with the lowest rate compared with Betadine andChloraPrep (3.9% vs. 6.4% vs. 7.1%, p = 0.002) [65]. Con-versely, a multicenter prospective RCT reported Chlora-Prep was associated with a lower rate of SSI thanBetadine (9.5% vs. 16.1%, p = 0.004, risk ratio 0.59, 95%CI 0.41-0.85) [66].As it stands, there is no clear evidence that one prep-

aration solution is the better choice in effectively lower-ing rate of SSI.• Wound irrigation:Wound irrigation is one of the oldest surgical mantras,

and many a medical student has heard their attendings

References

olonization may prevent nosocomial [47-49]

n of SSI rate with decolonization of [50]

s no evidence of clear benefit [51]

cloths on planned surgical sitesbacteria and may reduce SSI rate

[52-54]

nce that hair removal has any bearing on SSI rates [56]

o shaving, is associated with decreased incidence of SSIs


singsong “dilution is the solution to pollution”. Irrigationhelps to remove loose, necrotic tissue, particulate debris,and microorganisms from within the surgical site. It isconsidered the most important intraoperative step in re-ducing the risk of infection. Traditionally, sterile normalsaline has been used despite concrete, supporting evidence[67]. In fact, one prospective, randomized, double-blindedcontrolled study found that there was no statistically sig-nificant difference in rates of SSI between irrigation withsaline vs tap water [68].Irrigation with other solutions has also been suggested.

One prospective RCT looked at the efficacy of dilutebetadine irrigation (3.5% povidone-iodine solution) inthe prevention of postoperative infection in spinal surgery.The study demonstrated a remarkably lower infection ratewith dilute betadine solution (0%, n = 208) versus normalsaline irrigation (3.5%, n = 206) (p = 0.007) [69]. No ad-verse side effects or events were reported.• Thermoregulation:Intraoperative hypothermia has been shown to increase

the risk of SSIs, likely as a consequence of the reduction inperipheral circulation [70]. This reduction ultimately limitsoxygen concentrations in the tissues, especially in thewound, where the body needs it most to fight off infections.Moreover, hypothermia directly impairs immune function.Warming patients have been demonstrated to reduce in-fection rates in colorectal surgery [70]. Melling et al. [71]looked at warming patients before clean surgeries (locallyor systemically) and found the infection rate was 14% innon-warmed patients (19/139) versus 5% (13/277) inwarmed patients. Among warmed patients, the studydid not demonstrate a statistically significant differencein infection rates between local and systemic warming.These studies suggest that maintenance of periopera-

tive normothermia may be a worthwhile endeavor, espe-cially since it is easily implemented.• Antiseptic-coated sutures:Sutures coated with the antiseptic triclosan have been

developed to reduce SSIs. Edmiston et al. [72] evaluatedits effectiveness in inhibiting bacterial growth and adher-ence in an in vitro model. There was > 75% reduction ingram-positive and gram-negative bacterial adherence tothe antimicrobial suture. Clinically, in a prospective,double-blinded RCT in pediatric neurosurgical patients,Rozzelle et al. [73] demonstrated a statistically significantreduction in infection rates in those treated with anti-microbial suture (4.3% vs 21%, p = 0.038) undergoingcerebrospinal fluid shunt procedures. Unfortunately, thecost-effectiveness of these sutures is yet to be determined.The antiseptic-coated sutures cost 7% to 10% more thanstandard uncoated ones. Nevertheless, they may be justi-fied in high-risk patients, as was the case with Rozzelle’spatients, in which they underwent a procedure usually as-sociated with 5-15% risk of infection [73].

• Operating room traffic:Traffic in and out of the OR increases bacterial counts,

and has been demonstrated to increase infection rates.The opening and closing of doors likely disrupts the air-flow, allowing microbes to settle in the air directly abovethe surgical field. Panahi et al. [74] looked at the inci-dence of door opening during primary and revision totaljoint arthroplasty procedures. The study found that dooropenings averaged 0.65 and 0.84 per minute for primaryand revision procedures, respectively. The average totaldoor openings per procedure were 60 in primary casesand 135 in revisions [74].The intervention here is clearly to limit traffic flow.

This requires education and detailed communicationamong surgeons and OR personnel to aid preparation ofthe OR with essential instruments and components forscheduled procedures (Table 2).

Postoperative management• Drains and blood transfusions:A Cochrane review evaluated the occurrence of infec-

tions in relation to closed suction drainage after ortho-pedic surgery. 36 studies were included, involving 5464participants with 5697 surgical wounds identified [75].The meta-analysis demonstrated no statistically significantdifference in infection rates between those with drains andthose without. They concluded that there is no clear evi-dence that supports the routine use of closed suctiondrains in orthopedic surgery.The aforementioned study did however find that drain

use was often associated with the need for blood transfu-sions. Of course, blood transfusions carry its own risk ofinfections with blood-borne bacteria, viruses, or para-sites – albeit a very minimal one. The more pressing riskassociated with blood transfusions is the increasedlength of hospital stay and SSI [76]. It is thought thattransfusion evokes an immunomodulation, which affectswounds and increases risk of infection [77]. Bower et al.[78] found that patients who received transfusions werenearly twice as likely to have an infection than those thatdid not. More studies are needed to pin down whetherit’s a causal relationship or merely a confounding findingsuch that people who are at risk of needing a bloodtransfusion are equally at risk for SSIs.Regardless, blood transfusions do lead to an increased

length of stay as demonstrated by Weber et al. [76]. Thisin it of itself is a risk factor for infection, and every effortshould be made to judiciously discern the need for atransfusion. Preoperative assessment of hemoglobin andhematocrit levels and monitoring for symptomaticanemia rather than lab results alone would be beneficial.• Wound management:Postoperatively, the goal is to keep the surgical site

clean and dry. The CDC recommends surgical dressings

Table 2 Summary of intraoperative interventions

Intraoperative interventions Summary References

Prophylactic antibiotics ● Prophylactic antibiotics are effective in reducing SSI rates [57-62]

● Discontinue within 24 hours of closure to prevent superinfection

● Redosing may be beneficial for procedures > 4 hours or if EBL > 1.5 L

● Timing, duration, selection of antibiotics should be incorporated intothe “time-out” to improve compliance

Skin preparation ● No clear evidence that one preparation solution is superior [63-66]

Wound irrigation ● Important to remove loose, necrotic tissue, debris, andmicroorganisms from surgical site

[67-69]

● No difference in infection rates between saline and tap water

● Dilute betadine solution may be of benefit

Thermoregulation ● Maintaining perioperative normothermia may reduce SSI rates [70,71]

Antiseptic-coated sutures ● Effective in reducing SSI rates in neurosurgical patients,but cost-effectiveness has yet to be determined

[72,73]

Operating room traffic ● Limit OR traffic flow [74]


for 24–48 hours [79]. However, any soiled or blood-soaked dressings should be replaced immediately. Other-wise, any microorganisms nearby can become a sourceof infection. Dressings should also be chosen carefully toensure they stay intact.Antimicrobial dressings are available and they may

serve to reduce risk of infection. Silver-based dressings,in particular, have been shown to be effective in reducingthe rate of mediastinitis following cardiac surgery [80].Another common wound dressing is the use of nega-

tive pressure wound therapy. There is not much litera-ture on whether it helps decrease risks of infection. Butby drawing out fluid from the wound, completely sealingthe wound, and cutting down the frequency of dressingchanges, theoretically it should help reduce the inci-dence of SSIs.• Urinary tract infections:Although not strictly a SSI, urinary tract infections are

important to mention in the context of postoperativemanagement, since it is a common complication. Thedetails, however, are beyond the scope of this review.Some important principles to keep in mind are the follow-ing: avoid catherization when possible and remove as soonas possible; always practice aseptic technique during inser-tion and maintenance; consider the use of suprapubic andcondom catheters in lieu of urethral catheters, since theyhave a lower rate of infection [81]. Finally, in high-risk pa-tients, silver alloy catheters may have some antimicrobialbenefit [82] (Table 3).

Non-operative preventive measuresBriefly, we would like to mention some other preventivemeasures. These are not specifically related to SSIs butare more general measures. The multifactorial etiologyof health-care associated infections precludes successful

prevention in a vacuum of its subtypes (i.e. SSIs, UTIs,BSIs, PNEUs), so it is important to be cognizant of theseother measures. For more information, Curtis provides adetailed review on a number of these interventions [83].• Cleaning:Proper cleaning is an important aspect of preventing

health-care associated infections. Contaminated environ-mental surfaces often lead to cross-transmissions, andincrease rates of infection. Hospitals should train clean-ing personnel adequately, monitor performance regu-larly, and provide feedback. Moreover, they should makehospital cleaning personnel aware of their vital role inthe ultimate health of the patients. A prospective studyin Illinois compared rates of VRE infection before andafter a cleaning educational program. Rates of VRE in-fection fell by 64% [95% CI: 0.19-0.68] [84].There are few studies looking at which chemicals are

best to clean surfaces. However, some studies demon-strate the effectiveness of a bleach solution. One studycompared the use of 1:10 hypochlorite (bleach) solutionwith the use of a quaternary ammonium solution andfound that the former was associated with a significantlylower rate of C. difficile infection than the latter. An-other study found that unbuffered 1:10 hypochlorite so-lution reduced the frequency of positive C. difficilecultures in patient rooms from 31% to 16%. Finally, astudy of 17 rooms that housed VRE-positive patientsfound that prior to cleaning, 16/17 (94%) of the roomscontained viable VRE. After thorough cleaning with a 10%bleach solution, the amount of viable VRE decreased to 0(0%) (p < 0.001) [85].Hydrogen peroxide vapor has also been shown to be

an effective decontamination method. A British studycompared manual cleaning with hydrogen peroxide vapor.Prior to manual cleaning, in 10 surgical ward rooms, 89%

Table 3 Summary of postoperative interventions

Postoperative interventions Summary References

Drains and blood transfusion ● Cochrane review finds no difference in infection rates between those with drains and those without [75-78]

● Blood transfusions increase risk of infection and length of hospital stay

Wound management ● Keep surgical dressings clean and dry Antimicrobial dressings may help reduce infections [79,80]

Urinary tract infection ● Avoid catherization when possible, and always remove as soon as possible [81,82]

● Suprapubic and condom catheters have lower rates of infection

● In high-risk patients, silver alloy catheters may be of benefit


of 124 swab samples were positive for MRSA and 66%remained positive after manual cleaning. In comparison, 6other surgical ward rooms were swabbed and 72% of 85swabs were positive prior to cleaning. After hydrogen per-oxide treatment, only 1% of 85 remained positive [86]. An-other study investigated the feasibility of routine hydrogenperoxide decontamination in a busy hospital. One draw-back has always been the mean time for decontaminationwith hydrogen peroxide (~90-120 minutes). The studyconcluded that the additional time is offset by the drasticimprovement in surface hygiene, and reduction in nosoco-mial pathogens. They assert its feasibility in a busy hos-pital with a mean occupancy rate of 94% [87].• Waterborne transmission:Studies have found that the replacement of tap water

with sterile water for drinking, bathing, and procedurescan significantly reduce infection rates [19]. Other mea-sures include decontaminating the hospital water supply.This can be done by heating water to more than 50°C orwith UV light treatment, both of which has been shownto reduce levels of Legionella [88,89]. Another effectivemethod is copper-silver-based ionization systems, hasbeen shown to reduce molds and gram-negative bacteriasuch as P. aeuroginosa and Actinetobacter baumannii inaddition to Legionella [20,90,91]. One hospital found le-gionella infection rates drop from 2.45 cases to 0.18cases per 1000 discharges subsequent installation of acopper-silver ionization system [91].• Air filtration/treatment:High-efficiency particulate air filters can help reduce

aerosolized pathogens and decrease infection rates. Stud-ies have reported its use decreases airborne aspergillusconcentrations and aspergillus infections [92,93]. More-over, the use of portable filters has been demonstratedto significantly reduce airborne levels of MRSA and P.aeruginosa [94].Adequate outdoor air ventilation is also important to

help circulate and dilute air that may be ridden with air-borne pathogens. Indeed, poor ventilation is often asso-ciated with higher rates of acute respiratory disease [95].• Anti-microbial copper alloy:As mentioned above, touch surfaces are often a source of

contamination and cross-transmission. Surfaces can oftenharbor pathogens for days and even months, becoming a

reservoir of infection. Incorporating anti-microbial cop-per alloy into these surfaces has been suggested as apossible solution. Copper’s basic chemical properties andtendency to produce hydroxyl radicals and cations gives ita unique broad-spectrum biocidal ability. In vitro stud-ies have demonstrated its effectiveness in rapidly redu-cing bacterial concentration by 7 logs within just 2hours [96-98].A multi-center study looked at its clinical application

in the ICUs of 3 hospitals. Patients were randomlyassigned to rooms with and without copper alloy surfaces,and the rates of HAIs and/or colonization with MRSA orVRE were compared. Six objects were fabricated fromcopper alloy, four of which were identical among thethree hospitals: bed rails, overbed tables, IV poles, andarms of visitor’s chair. Results indicated that the rate ofHAI and/or MRSA or VRE colonization in copper roomswere significantly lower than non-copper rooms (0.071 vs.0.123, p = 0.020). The rate for just HAI was decreased58% from 0.081 to 0.034 (p = 0.013) [98].Another study found that the combined burden of

MRSA and VRE were 96.8% lower on copper surfacesthan current plastic, wood, metal, and painted surfaces.Copper surfaces were also found to continuously limitmicrobial bioburden, achieving same levels as terminalcleaning [99]. Copper-alloy surfaces are proving to be apromising intervention (Table 4).

DevelopmentsAt Brigham and Women’s Hospital, in the Laboratoryfor Tissue Repair and Gene Transfer, we have developeda wound enclosure device, which we have previouslyshown to be a promising wound healing modality with-out any adverse side effects [100-103]. It consists of apolyurethane chamber that envelops the wounds, creat-ing a controlled incubator-like microenvironment. Thisplatform allows us to maintain optimal conditions forwound healing while concomitantly providing both top-ical antibiotics and analgesics to the wound [100-103].In addition to wound healing improvement, we have re-alized its potential as a novel intervention for health-care associated surgical site infections. These chamberseliminate the need for daily dressing changes, since fluidcan easily be aspirated and sampled from the chamber

Table 4 Summary of non-operative preventive measures

Non-operative preventive measures Summary References

Cleaning ● Hospital cleaning personnel should be made aware of their vital rolein decreasing HAIs; they should be trained appropriately, adequately, and monitored

[84-87]

● Bleach solutions and hydrogen peroxide vapor have been shown to be effectivedecontaminating agents

Waterborne transmission ● Replacement of tap water with sterile water may reduce infection rates [88-91]

● Decontaminating hospital water supply may be an alternative

Air filtration ● High-efficiency particulate air filters can help reduce airborne levels of aspergillus,MRSA, and P. aeruginosa

[92-95]

Anti-microbial copper alloy ● Incorporating copper-alloy in hospital surfaces may limit contaminationand cross-transmission

[96-99]


itself, and the clear chamber allows easy visual inspec-tion of the wounds, facilitating hospital rounds. Thiswould significantly decrease the risk of contaminationfrom hospital personnel.Using a porcine model, we have been able to dramatic-

ally decrease bacteria concentrations in both wound fluidand tissue by adding topical antibiotics (up to 1,000 min-imal inhibitory concentration) within our wound cham-bers, even after inoculation of wounds with 108 colonyforming units/mL (unpublished data). Moreover, ourpreliminary studies indicate its ability to rapidly de-crease bacterial counts of endogenous flora. This hasgreat implications, since, as mentioned, endogenousflora is a common source of contamination that leads toSSI. Similar to the antiseptic skin cloths discussed above,which have been shown to reduce infection rates, thesechambers may be a safe, more efficacious alternative. The-oretically, these chambers could be placed preoperativelyon the surgical site to rapidly decolonize endogenousflora, and also be placed as a wound dressing post-operatively to further prevent SSIs. Further studies areplanned, but at this point, it looks to be a promisingnovel intervention that could easily be implemented.

Numbers and costsUsing data from the National Nosocomial InfectionsSurveillance (NNIS) system, National Hospital DischargeSurvey (NHDS), and the American Hospital Association(AHA) Survey, Klevens et al. estimated 1.7 million HAIsoccurred in U.S. hospitals in 2002. Among these, ap-proximately 155,000 deaths occurred, 99,000 of whichwere considered caused by or significantly associated withthe HAI [3]. This puts HAIs in the top ten leading causesof death, compared to CDC’s 2010 data for Alzheimer’sdisease (83,494), diabetes (69,071), and kidney diseases(50,476) [104]. In another study, Scott et al. estimated thatthe annual direct cost of HAIs to U.S. hospitals rangesfrom $28.4 to $45 billion [4]. With a high estimate that70% of HAIs are preventable by current available strat-egies, the economic benefits of prevention ranges from$25.0 to $31.5 billion. With a low estimate that 20% are

preventable, the savings range from $5.7 to $6.8 billion,which is still comparable to the healthcare costs ofstroke ($6.7 billion), diabetes mellitus with complica-tions ($4.5 billion), and chronic obstructive lung disease(4.2 billion) [105].Surgical site infections alone account for roughly

290,000 of the total HAIs, and are estimated to cause8,000 deaths, a case fatality rate of 2.8%. They are thesecond most frequently reported HAI [3]. As for the at-tributable costs of SSIs, Anderson et al. gives a low esti-mate of $10,443 per infection and Stone et al. gives it ahigh estimate of $25,546 per infection [55,106]. From apatient perspective, wound infections are the secondmost commonly experienced adverse event (14%), sec-ond only to medication errors (19%) [107]. Commonly,SSIs increase the hospital length of stay (LOS) on aver-age between 7.3 days and 14.3 days [108]. Moreover,they increase the risk of re-admittance within 30 days by5 times, double the mortality rate, and decrease qualityof life [109,110]. In a systematic review, Umscheid et al.estimated that as much as 55% of SSIs may be prevent-able. This would equate to approximately 75,526 to156,862 preventable infections per year and subse-quently, 2,133 to 4,431 preventable deaths [111].

Final thoughtsSurgical site infections remain a tremendous issue in the21st century. There are several successful preventive mea-sures described in the literature; however, an institution-wide adoption of several of these interventions is oftenfew and far between. Complacency in this matter is almosttantamount to negligence. In the spirit of primum nonnocera, we should ever strive to aggressively lower infec-tion rates as much as we can. Additionally, with the rap-idly changing climate of our healthcare industry, wherethe way we practice and the quality of our care is increas-ingly scrutinized, infection prevention should be an ut-most priority.Although, it is doubtful one single preventive measure

will ever be the be-all and end-all for our problems, thereis hope that bundles of multiple measures can dramatically

Tsai and Caterson Patient Safety in Surgery 2014, 8:42 0 of 13http://www.pssjournal.com/content/8/1/42

reduce the rate of SSIs – a testament to Aristotle’s “thewhole is greater than the sum of its parts” [112-114].Alexander et al. suggests that adherence to current guide-lines and available interventions can reduce infection ratesto less than 0.5% in clean wounds, less than 1% in cleancontaminated wounds, and less than 2% in highly contam-inated wounds [115]. With a similar mindset, the MayoClinic in Florida instituted multiple interventions as anSSI Bundle. Thompson et al. [116] details their institu-tion’s experience and results in their paper aptly titled,“Chasing Zero”. During the study period between May2008 and June 2010, they achieved a 57% decrease in SSIrate with an estimated savings of nearly $1 million (Class ISSI, clean wounds, rate from 1.78% to 0.51% and Class IISSI, clean-contaminated, rate from 2.82% to 1.44%) [116].

ConclusionHealth-care associated infections continue to cause sig-nificant patient morbidity and mortality and account fora great deal of healthcare costs. Nevertheless, we are op-timistic that together we are ever moving towards im-proving patient care. Though many successful preventivemeasures exist, more can always be done in terms of re-search and practicing evidence-based care. We believethat pushing for an organized institution-wide adoptionof multiple interventions may be the key to reducing in-fection rates. No doubt each institution differs in cap-acity and resources, so a discussion is necessary at eachinstitution on what is feasible. We hope this review andthe work of many others before us can help inspire add-itional dialogue regarding this matter.

AbbreviationsHAI: Healthcare-associated infection; SSI: Surgical site infection; CDC:Centers for disease control; NHSN: National healthcare safety network;UTI: Urinary tract infections; BSI: Bloodstream infections; PNEU: Pneumonia;MRSA: Methicillin-resistant staphylococcus aureus; VRE: Vancomycin-resistantenterococci faecium; CHG: Chlorhexidine gluconate; RCT: Randomizedcontrolled trial.

Competing interestsThe authors declare that they have no competing interests.

Authors’ contributionsAll authors participated in study conception and design. DT carried outliterature search, analysis, and interpretation, and drafted the manuscript. EJcontributed to literature search, analysis, interpretation, and participated incritical revision. All authors read and approved the final manuscript.

Received: 18 June 2014 Accepted: 23 September 2014

References1. Millard C: Destiny of the Republic: A Tale of Madness, Medicine and the Murder

of a President. Knopf Doubleday Publishing Group; 2012.2. Clark FC: A brief history of antiseptic surgery. Med Libr Hist J 1907,

5:145–172.3. Klevens RM, Edwards JR, Richards CL Jr, Horan TC, Gaynes RP, Pollock DA,

Cardo DM: Estimating health care-associated infections and deaths in U.S. hospitals, 2002. Public Health Rep 2007, 122:160–166.

4. Scott RD, Douglas R: The Direct Medical Costs of Healthcare-AssociatedInfections in US Hospitals and the Benefits of Prevention; 2009.

5. Locksley RM, Cohen ML, Quinn TC, Tompkins LS, Coyle MB, Kirihara JM,Counts GW: Multiply antibiotic-resistant Staphylococcus aureus:introduction, transmission, and evolution of nosocomial infection.Ann Intern Med 1982, 97:317–324.

6. Horan TC, Andrus M, Dudeck MA: CDC/NHSN surveillance definition ofhealth care-associated infection and criteria for specific types of infectionsin the acute care setting. Am J Infect Control 2008, 36:309–332.

7. Horan TC, Gaynes RP, Martone WJ, Jarvis WR, Emori TG: CDC definitions ofnosocomial surgical site infections, 1992: a modification of CDCdefinitions of surgical wound infections. Infect Control Hosp Epidemiol1992, 13:606–608.

8. McGowan JE Jr: Changing etiology of nosocomial bacteremia andfungemia and other hospital-acquired infections. Rev Infect Dis 1985,7(Suppl 3):S357–S370.

9. Owens CD, Stoessel K: Surgical site infections: epidemiology,microbiology and prevention. J Hosp Infect 2008, 70(Suppl 2):3–10.

10. Altemeier WA, Culbertson WR, Hummel RP: Surgical considerations ofendogenous infections–sources, types, and methods of control. Surg ClinNorth Am 1968, 48:227–240.

11. Evans CA, Smith WM, Johnston EA, Giblett ER: Bacterial flora of the normalhuman skin. J Invest Dermatol 1950, 15:305–324.

12. Chiller K, Selkin BA, Murakawa GJ: Skin microflora and bacterial infectionsof the skin. J Invest Derm Symp Proc 2001, 6:170–174.

13. Turnbaugh PJ, Ley RE, Hamady M, Fraser-Liggett CM, Knight R, Gordon JI:The human microbiome project. Nature 2007, 449(7164):804–810.

14. Wong VW, Martindale RG, Longaker MT, Gurtner GC: From germ theory togerm therapy: skin microbiota, chronic wounds, and probiotics. PlastReconstr Surg 2013, 132:854e–861e.

15. Rosenthal M, Goldberg D, Aiello A, Larson E, Foxman B: Skin microbiota:microbial community structure and its potential association with healthand disease. Infect Genet Evol 2011, 11:839–848.

16. Talmor M, Barie PS: Microbiota in “austere” environments: belly buttonbanter and other (navel) fluff. Surg Infect (Larchmt) 2011, 12:427–428.

17. Hidron AI, Edwards JR, Patel J, Horan TC, Sievert DM, Pollock DA, Fridkin SK,National Healthcare Safety Network T, Participating National HealthcareSafety Network F: NHSN annual update: antimicrobial-resistant pathogensassociated with healthcare-associated infections: annual summary ofdata reported to the National Healthcare Safety Network at the Centersfor Disease Control and Prevention, 2006–2007. Infect Control HospEpidemiol 2008, 29:996–1011.

18. Kim DH, Spencer M, Davidson SM, Li L, Shaw JD, Gulczynski D, Hunter DJ,Martha JF, Miley GB, Parazin SJ, Dejoie P, Richmond JC: Institutionalprescreening for detection and eradication of methicillin-resistantStaphylococcus aureus in patients undergoing elective orthopaedicsurgery. J Bone Joint Surg Am 2010, 92:1820–1826.

19. Anaissie EJ, Penzak SR, Dignani MC: The hospital water supply as a sourceof nosocomial infections: a plea for action. Arch Intern Med 2002,162:1483.

20. Pedro-Botet ML, Sanchez I, Sabria M, Sopena N, Mateu L, Garcia-Nunez M, Rey-Joly C: Impact of copper and silver ionization on fungalcolonization of the water supply in health care centers: implications forimmunocompromised patients. Clin Infect Dis 2007, 45:84–86.

21. Warris A, Onken A, Gaustad P, Janssen W, van der Lee H, Verweij PE,Abrahamsen TG: Point-of-use filtration method for the prevention offungal contamination of hospital water. J Hosp Infect 2010, 76:56–59.

22. Jones JS, Hoerle D, Riekse R: Stethoscopes: a potential vector of infection?Ann Emerg Med 1995, 26:296–299.

23. Smith MA, Mathewson JJ, Ulert IA, Scerpella EG, Ericsson CD: Contaminatedstethoscopes revisited. Arch Intern Med 1996, 156:82–84.

24. Bernard L, Kereveur A, Durand D, Gonot J, Goldstein F, Mainardi JL, Acar J,Carlet J: Bacterial contamination of hospital physicians’ stethoscopes.Infect Control Hosp Epidemiol 1999, 20:626–628.

25. Bosco JA 3rd, Slover JD, Haas JP: Perioperative strategies for decreasinginfection: a comprehensive evidence-based approach. Instr Course Lect2010, 59:619–628.

26. Savage JW, Anderson PA: An update on modifiable factors to reduce therisk of surgical site infections. Spine J 2013, 13(9):1017–1029.

27. Fletcher N, Sofianos D, Berkes MB, Obremskey WT: Prevention ofperioperative infection. J Bone Joint Surg Am 2007, 89:1605–1618.


28. WHO Guidelines on Hand Hygiene in Health Care: First Global Patient SafetyChallenge Clean Care is Safer Care. Geneva: WHO Guidelines Approved bythe Guidelines Review Committee; 2009.

29. Allegranzi B, Gayet-Ageron A, Damani N, Bengaly L, McLaws ML,Moro ML, Memish Z, Urroz O, Richet H, Storr J, Donaldson L, Pittet D:Global implementation of WHO’s multimodal strategy for improvementof hand hygiene: a quasi-experimental study. Lancet Infect Dis 2013,13:843–851.

30. Sax H, Allegranzi B, Uckay I, Larson E, Boyce J, Pittet D: ‘My five momentsfor hand hygiene’: a user-centred design approach to understand, train,monitor and report hand hygiene. J Hosp Infect 2007, 67:9–21.

31. Bryce EA, Spence D, Roberts FJ: An in-use evaluation of an alcohol-basedpre-surgical hand disinfectant. Infect Control Hosp Epidemiol 2001,22:635–639.

32. Parienti JJ, Thibon P, Heller R, Le Roux Y, von Theobald P, Bensadoun H,Bouvet A, Lemarchand F, Le Coutour X, Antisepsie Chirurgicale des mainsStudy G: Hand-rubbing with an aqueous alcoholic solution vs traditionalsurgical hand-scrubbing and 30-day surgical site infection rates:a randomized equivalence study. JAMA 2002, 288:722–727.

33. Grabsch EA, Mitchell DJ, Hooper J, Turnidge JD: In-use efficacy of achlorhexidine in alcohol surgical rub: a comparative study. ANZ J Surg2004, 74:769–772.

34. Tanner J, Swarbrook S, Stuart J: Surgical hand antisepsis to reduce surgicalsite infection. Cochrane Database Syst Rev 2008, 23(1):CD00428.

35. Braun SD, Monecke S, Thurmer A, Ruppelt A, Makarewicz O, Pletz M,Reibetaig A, Slickers P, Ehricht R: Rapid identification of carbapenemasegenes in gram-negative bacteria with an oligonucleotide microarray-based assay. PLoS One 2014, 9:e102232.

36. Caliendo AM: Multiplex PCR and emerging technologies forthe detection of respiratory pathogens. Clin Infect Dis 2011,52(Suppl 4):S326–S330.

37. Foxman B, Goldberg D, Murdock C, Xi C, Gilsdorf JR: Conceptualizinghuman microbiota: from multicelled organ to ecological community.Interdiscip Perspect Infect Dis 2008, 2008:613979.

38. Huebinger RM, Liu MM, Dowd SE, Rivera-Chavez FA, Boynton J, Carey C,Hawkins K, Minshall CT, Wolf SE, Minei JP, Barber RC: Examination withnext-generation sequencing technology of the bacterial microbiota inbronchoalveolar lavage samples after traumatic injury. Surg Infect(Larchmt) 2013, 14:275–282.

39. Kobayashi N, Bauer TW, Tuohy MJ, Fujishiro T, Procop GW: Briefultrasonication improves detection of biofilm-formative bacteria arounda metal implant. Clin Orthop Relat Res 2007, 457:210–213.

40. Malic S, Hill KE, Hayes A, Percival SL, Thomas DW, Williams DW: Detectionand identification of specific bacteria in wound biofilms using peptidenucleic acid fluorescent in situ hybridization (PNA FISH). Microbiology2009, 155:2603–2611.

41. Perl TM, Golub JE: New approaches to reduce Staphylococcus aureusnosocomial infection rates: treating S. aureus nasal carriage. AnnPharmacother 1998, 32:S7–S16.

42. Kluytmans J, van Belkum A, Verbrugh H: Nasal carriage of Staphylococcusaureus: epidemiology, underlying mechanisms, and associated risks. ClinMicrobiol Rev 1997, 10:505–520.

43. Wenzel RP, Perl TM: The significance of nasal carriage of Staphylococcusaureus and the incidence of postoperative wound infection. J Hosp Infect1995, 31:13–24.

44. Mest DR, Wong DH, Shimoda KJ, Mulligan ME, Wilson SE: Nasalcolonization with methicillin-resistant Staphylococcus aureus onadmission to the surgical intensive care unit increases the risk ofinfection. Anesth Analg 1994, 78:644–650.

45. Pujol M, Pena C, Pallares R, Ariza J, Ayats J, Dominguez MA, Gudiol F:Nosocomial Staphylococcus aureus bacteremia among nasal carriers ofmethicillin-resistant and methicillin-susceptible strains. Am J Med 1996,100:509–516.

46. Campbell W, Hendrix E, Schwalbe R, Fattom A, Edelman R: Head-injuredpatients who are nasal carriers of Staphylococcus aureus are at high riskfor Staphylococcus aureus pneumonia. Crit Care Med 1999, 27:798–801.

47. Perl TM, Cullen JJ, Wenzel RP, Zimmerman MB, Pfaller MA, Sheppard D,Twombley J, French PP, Herwaldt LA, Mupirocin and The Risk OfStaphylococcus Aureus Study T: Intranasal mupirocin to preventpostoperative Staphylococcus aureus infections. N Engl J Med 2002,346:1871–1877.

48. Bode LG, Kluytmans JA, Wertheim HF, Bogaers D, Vandenbroucke-GraulsCM, Roosendaal R, Troelstra A, Box AT, Voss A, van der Tweel I, van BelkumA, Verbrugh HA, Vos MC: Preventing surgical-site infections in nasalcarriers of Staphylococcus aureus. N Engl J Med 2010, 362:9–17.

49. Rao N, Cannella BA, Crossett LS, Yates AJ Jr, McGough RL 3rd, Hamilton CW:Preoperative screening/decolonization for Staphylococcus aureus toprevent orthopedic surgical site infection: prospective cohort study with2-year follow-up. J Arthroplasty 2011, 26:1501–1507.

50. Portigliatti Barbos M, Mognetti B, Pecoraro S, Picco W, Veglio V:Decolonization of orthopedic surgical team S. aureus carriers: impact onsurgical-site infections. J Orthop Traumatol 2010, 11:47–49.

51. Webster J, Osborne S: Preoperative bathing or showering with skinantiseptics to prevent surgical site infection. Cochrane Database Syst Rev2012, 9, CD004985.

52. Murray MR, Saltzman MD, Gryzlo SM, Terry MA, Woodward CC, Nuber GW:Efficacy of preoperative home use of 2% chlorhexidine gluconate clothbefore shoulder surgery. J Shoulder Elbow Surg 2011, 20:928–933.

53. Eiselt D: Presurgical skin preparation with a novel 2% chlorhexidinegluconate cloth reduces rates of surgical site infection in orthopaedicsurgical patients. Orthop Nurs 2009, 28:141–145.

54. Graling PR, Vasaly FW: Effectiveness of 2% CHG cloth bathing forreducing surgical site infections. AORN J 2013, 97:547–551.

55. Stone PW, Braccia D, Larson E: Systematic review of economic analyses ofhealth care-associated infections. Am J Infect Control 2005, 33:501–509.

56. Tanner J, Woodings D, Moncaster K: Preoperative hair removal to reducesurgical site infection. Cochrane Database Syst Rev 2006, 3:CD004122.

57. Barker FG 2nd: Efficacy of prophylactic antibiotic therapy in spinalsurgery: a meta-analysis. Neurosurgery 2002, 51:391–400. discussion400–391.

58. Henley MB, Jones RE, Wyatt RW, Hofmann A, Cohen RL: Prophylaxis withcefamandole nafate in elective orthopedic surgery. Clin Orthop Relat Res1986, 209:249–254.

59. Lidwell OM, Elson RA, Lowbury EJ, Whyte W, Blowers R, Stanley SJ, Lowe D:Ultraclean air and antibiotics for prevention of postoperative infection Amulticenter study of 8,052 joint replacement operations. Acta OrthopScand 1987, 58:4–13.

60. Slobogean GP, Kennedy SA, Davidson D, O’Brien PJ: Single- versusmultiple-dose antibiotic prophylaxis in the surgical treatment of closedfractures: a meta-analysis. J Orthop Trauma 2008, 22:264–269.

61. Dehne MG, Muhling J, Sablotzki A, Nopens H, Hempelmann G:Pharmacokinetics of antibiotic prophylaxis in major orthopedic surgeryand blood-saving techniques. Orthopedics 2001, 24:665–669.

62. Rosenberg AD, Wambold D, Kraemer L, Begley-Keyes M, Zuckerman SL,Singh N, Cohen MM, Bennett MV: Ensuring appropriate timing ofantimicrobial prophylaxis. J Bone Joint Surg Am 2008, 90:226–232.

63. Ostrander RV, Botte MJ, Brage ME: Efficacy of surgical preparation solutionsin foot and ankle surgery. J Bone Joint Surg Am 2005, 87:980–985.

64. Savage JW, Weatherford BM, Sugrue PA, Nolden MT, Liu JC, Song JK, HaakMH: Efficacy of surgical preparation solutions in lumbar spine surgery.J Bone Joint Surg Am 2012, 94:490–494.

65. Swenson BR, Hedrick TL, Metzger R, Bonatti H, Pruett TL, Sawyer RG: Effectsof preoperative skin preparation on postoperative wound infectionrates: a prospective study of 3 skin preparation protocols. Infect ControlHosp Epidemiol 2009, 30:964–971.

66. Darouiche RO, Wall MJ Jr, Itani KM, Otterson MF, Webb AL, Carrick MM,Miller HJ, Awad SS, Crosby CT, Mosier MC, Alsharif A, Berger DH:Chlorhexidine-Alcohol versus Povidone-Iodine for Surgical-SiteAntisepsis. N Engl J Med 2010, 362:18–26.

67. Fernandez R, Griffiths R: Water for wound cleansing. Cochrane DatabaseSyst Rev 2012, 2, CD003861.

68. Weiss EA, Oldham G, Lin M, Foster T, Quinn JV: Water is a safe andeffective alternative to sterile normal saline for wound irrigation prior tosuturing: a prospective, double-blind, randomised, controlled clinicaltrial. BMJ Open 2013, 3(1). doi:10.1136/bmjopen-2012-001504.

69. Cheng MT, Chang MC, Wang ST, Yu WK, Liu CL, Chen TH: Efficacy of dilutebetadine solution irrigation in the prevention of postoperative infectionof spinal surgery. Spine 2005, 30:1689–1693.

70. Kurz A, Sessler DI, Lenhardt R: Perioperative normothermia to reduce theincidence of surgical-wound infection and shorten hospitalization. Studyof Wound Infection and Temperature Group. N Engl J Med 1996,334:1209–1215.


71. Melling AC, Ali B, Scott EM, Leaper DJ: Effects of preoperative warming onthe incidence of wound infection after clean surgery: a randomisedcontrolled trial. Lancet 2001, 358:876–880.

72. Edmiston CE, Seabrook GR, Goheen MP, Krepel CJ, Johnson CP, Lewis BD,Brown KR, Towne JB: Bacterial adherence to surgical sutures: canantibacterial-coated sutures reduce the risk of microbial contamination?J Am Coll Surg 2006, 203:481–489.

73. Rozzelle CJ, Leonardo J, Li V: Antimicrobial suture wound closure forcerebrospinal fluid shunt surgery: a prospective, double-blinded,randomized controlled trial. J Neurosurg Pediatr 2008, 2:111–117.

74. Panahi P, Stroh M, Casper DS, Parvizi J, Austin MS: Operating room traffic isa major concern during total joint arthroplasty. Clin Orthop Relat Res 2012,470:2690–2694.

75. Parker MJ, Livingstone V, Clifton R, McKee A: Closed suction surgicalwound drainage after orthopaedic surgery. Cochrane Database Syst Rev2007, 3:CD001825.

76. Weber EW, Slappendel R, Prins MH, van der Schaaf DB, Durieux ME,Strumper D: Perioperative blood transfusions and delayedwound healing after hip replacement surgery: effects onduration of hospitalization. Anesth Analg 2005, 100:1416–1421.table of contents.

77. Vamvakas EC, Blajchman MA: Transfusion-related immunomodulation(TRIM): an update. Blood Rev 2007, 21:327–348.

78. Bower WF, Cheung CS, Lai RW, Underwood MJ, van Hasselt CA: An audit ofrisk factors for wound infection in patients undergoing coronary arterybypass grafting or valve replacement. Hong Kong Med J 2008, 14:371–378.

79. Mangram AJ, Horan TC, Pearson ML, Silver LC, Jarvis WR: Guideline forprevention of surgical site infection, 1999. Hospital Infection ControlPractices Advisory Committee. Infect Control Hosp Epidemiol 1999,20:250–278. quiz 279–280.

80. Huckfeldt R, Redmond C, Mikkelson D, Finley PJ, Lowe C, Robertson J:A clinical trial to investigate the effect of silver nylon dressings onmediastinitis rates in postoperative cardiac sternotomy incisions.Ostomy Wound Manage 2008, 54:36–41.

81. Gould CV, Umscheid CA, Agarwal RK, Kuntz G, Pegues DA, HealthcareInfection Control Practices Advisory C: Guideline for prevention ofcatheter-associated urinary tract infections 2009. Infect Control HospEpidemiol 2010, 31:319–326.

82. Saint S, Lipsky BA: Preventing catheter-related bacteriuria: should we?Can we? How? Arch Intern Med 1999, 159:800–808.

83. Curtis LT: Prevention of hospital-acquired infections: review ofnon-pharmacological interventions. J Hosp Infect 2008, 69:204–219.

84. Hayden MK, Bonten MJ, Blom DW, Lyle EA, van de Vijver DA, Weinstein RA:Reduction in acquisition of vancomycin-resistant enterococcus afterenforcement of routine environmental cleaning measures. Clin Infect Dis2006, 42:1552–1560.

85. Eckstein BC, Adams DA, Eckstein EC, Rao A, Sethi AK, Yadavalli GK, DonskeyCJ: Reduction of Clostridium Difficile and vancomycin-resistant Enterococcuscontamination of environmental surfaces after an intervention to improvecleaning methods. BMC Infect Dis 2007, 7:61.

86. French GL, Otter JA, Shannon KP, Adams NM, Watling D, Parks MJ: Tacklingcontamination of the hospital environment by methicillin-resistantStaphylococcus aureus (MRSA): a comparison between conventionalterminal cleaning and hydrogen peroxide vapour decontamination.J Hosp Infect 2004, 57:31–37.

87. Otter JA, Puchowicz M, Ryan D, Salkeld JA, Cooper TA, Havill NL, Tuozzo K,Boyce JM: Feasibility of routinely using hydrogen peroxide vapor todecontaminate rooms in a busy United States hospital. Infect ControlHosp Epidemiol 2009, 30:574–577.

88. Sabria M, Yu VL: Hospital-acquired legionellosis: solutions for apreventable infection. Lancet Infect Dis 2002, 2:368–373.

89. Farr BM, Gratz JC, Tartaglino JC, Getchell-White SI, Groschell DH: Evaluationof ultraviolet light for disinfection of hospital water contaminated withLegionella. Lancet 1988, 2:669–672.

90. Huang HI, Shih HY, Lee CM, Yang TC, Lay JJ, Lin YE: In vitro efficacyof copper and silver ions in eradicating Pseudomonas aeruginosa,Stenotrophomonas maltophilia and Acinetobacter baumannii:implications for on-site disinfection for hospital infection control.Water Res 2008, 42:73–80.

91. Modol J, Sabria M, Reynaga E, Pedro-Botet ML, Sopena N, Tudela P, Casas I,Rey-Joly C: Hospital-acquired legionnaires disease in a university hospital:

impact of the copper-silver ionization system. Clin Infect Dis 2007,44:263–265.

92. Hahn T, Cummings KM, Michalek AM, Lipman BJ, Segal BH, McCarthy PL Jr:Efficacy of high-efficiency particulate air filtration in preventingaspergillosis in immunocompromised patients with hematologicmalignancies. Infect Control Hosp Epidemiol 2002, 23:525–531.

93. Loo VG, Bertrand C, Dixon C, Vitye D, DeSalis B, McLean AP, Brox A, RobsonHG: Control of construction-associated nosocomial aspergillosis in anantiquated hematology unit. Infect Control Hosp Epidemiol 1996, 17:360–364.

94. Boswell TC, Fox PC: Reduction in MRSA environmental contaminationwith a portable HEPA-filtration unit. J Hosp Infect 2006, 63:47–54.

95. Brundage JF, Scott RM, Lednar WM, Smith DW, Miller RN: Building-associated risk of febrile acute respiratory diseases in Army trainees.JAMA 1988, 259:2108–2112.

96. Warnes SL, Green SM, Michels HT, Keevil CW: Biocidal efficacy of copperalloys against pathogenic enterococci involves degradation of genomicand plasmid DNAs. Appl Environ Microbiol 2010, 76:5390–5401.

97. Weaver L, Noyce JO, Michels HT, Keevil CW: Potential action of coppersurfaces on meticillin-resistant Staphylococcus aureus. J Appl Microbiol2010, 109:2200–2205.

98. Salgado CD, Sepkowitz KA, John JF, Cantey JR, Attaway HH, Freeman KD,Sharpe PA, Michels HT, Schmidt MG: Copper surfaces reduce the rate ofhealthcare-acquired infections in the intensive care unit. Infect ControlHosp Epidemiol 2013, 34:479–486.

99. Schmidt MG, Attaway Iii HH, Fairey SE, Steed LL, Michels HT, Salgado CD:Copper continuously limits the concentration of bacteria resident onbed rails within the intensive care unit. Infect Control Hosp Epidemiol 2013,34:530–533.

100. Breuing K, Eriksson E, Liu P, Miller DR: Healing of partial thickness porcineskin wounds in a liquid environment. J Surg Res 1992, 52:50–58.

101. Svensjo T, Pomahac B, Yao F, Slama J, Eriksson E: Accelerated healing offull-thickness skin wounds in a wet environment. Plast Reconstr Surg 2000,106:602–612. discussion 613–604.

102. Velander P, Theopold C, Bleiziffer O, Bergmann J, Svensson H, Feng Y,Eriksson E: Cell suspensions of autologous keratinocytes or autologousfibroblasts accelerate the healing of full thickness skin wounds in adiabetic porcine wound healing model. J Surg Res 2009, 157:14–20.

103. Eriksson E, Perez N, Slama J, Page CP, Andree C, Maguire JH: Treatment ofchronic, nonhealing abdominal wound in a liquid environment. Ann PlastSurg 1996, 36:80–83.

104. Sherry L, Murphy BSJX MD, Kenneth D, Kochanek MA: Deaths: Final Data for2010. U.S. Department of Health and Human Services; 2013.

105. Levit KSE, Ryank K, Elixhauser A: HCUP Facts and Figures, 2006: Statistics onHospital-Based Care in the United States. Rockville (MD): HCUP Facts andFigures; 2008.

106. Anderson DJ, Kirkland KB, Kaye KS, Thacker PA 2nd, Kanafani ZA, Auten G,Sexton DJ: Underresourced hospital infection control and preventionprograms: penny wise, pound foolish? Infect Control Hosp Epidemiol 2007,28:767–773.

107. Leape LL, Brennan TA, Laird N, Lawthers AG, Localio AR, Barnes BA, HebertL, Newhouse JP, Weiler PC, Hiatt H: The nature of adverse events inhospitalized patients. Results of the Harvard Medical Practice Study II.N Engl J Med 1991, 324:377–384.

108. Vegas AA, Jodra VM, Garcia ML: Nosocomial infection in surgery wards: acontrolled study of increased duration of hospital stays and direct costof hospitalization. Eur J Epidemiol 1993, 9:504–510.

109. Kirkland KB, Briggs JP, Trivette SL, Wilkinson WE, Sexton DJ: The impact ofsurgical-site infections in the 1990s: attributable mortality, excess lengthof hospitalization, and extra costs. Infect Control Hosp Epidemiol 1999,20:725–730.

110. Whitehouse JD, Friedman ND, Kirkland KB, Richardson WJ, Sexton DJ: Theimpact of surgical-site infections following orthopedic surgery at a communityhospital and a university hospital: adverse quality of life, excess lengthof stay, and extra cost. Infect Control Hosp Epidemiol 2002, 23:183–189.

111. Umscheid CA, Mitchell MD, Doshi JA, Agarwal R, Williams K, Brennan PJ:Estimating the proportion of healthcare-associated infections that arereasonably preventable and the related mortality and costs. Infect ControlHosp Epidemiol 2011, 32:101–114.

112. Bratzler DW, Hunt DR: The surgical infection prevention and surgical careimprovement projects: national initiatives to improve outcomes forpatients having surgery. Clin Infect Dis 2006, 43:322–330.


113. Dellinger EP, Hausmann SM, Bratzler DW, Johnson RM, Daniel DM, Bunt KM,Baumgardner GA, Sugarman JR: Hospitals collaborate to decrease surgicalsite infections. Am J Surg 2005, 190:9–15.

114. Stulberg JJ, Delaney CP, Neuhauser DV, Aron DC, Fu P, Koroukian SM:Adherence to surgical care improvement project measures and theassociation with postoperative infections. JAMA 2010, 303:2479–2485.

115. Alexander JW, Solomkin JS, Edwards MJ: Updated recommendations forcontrol of surgical site infections. Ann Surg 2011, 253:1082–1093.

116. Thompson KM, Oldenburg WA, Deschamps C, Rupp WC, Smith CD: Chasingzero: the drive to eliminate surgical site infections. Ann Surg 2011,254:430–436. discussion 436–437.

doi:10.1186/s13037-014-0042-5Cite this article as: Tsai and Caterson: Current preventive measures forhealth-care associated surgical site infections: a review. Patient Safety inSurgery 2014 8:42.

Submit your next manuscript to BioMed Centraland take full advantage of:

• Convenient online submission

• Thorough peer review

• No space constraints or color figure charges

• Immediate publication on acceptance

• Inclusion in PubMed, CAS, Scopus and Google Scholar

• Research which is freely available for redistribution

Submit your manuscript at www.biomedcentral.com/submit

Reproduced with permission of the copyright owner. Further reproduction prohibited withoutpermission.

s13037-014-0042-5.pdf

Tsai and Caterson Patient Safety in Surgery 2014, 8:42 of 13http://www.pssjournal.com/content/8/1/42

Even with standard wound precautions, this antibiotic-resistant S. aureus was transmitted to 34 other patients.Ultimately, 27 were infected and 17 of the 34 died [5].At present we live in a world of unparalleled capability

in science, technology, and medicine. Things that wereonce only imagined in fiction and sci-fi movies arequickly becoming our reality. Not only do we routinelyperform heart and lung transplants, but we have enteredthe realm of face and hand transplantation. Despite allthese advances, health-care associated infections have re-peatedly proven to remain a formidable force that loomsin the background—one that if we don’t actively andcontinually combat can threaten to undo any good westrive to accomplish.

DefinitionHealthcare-associated infection is officially defined bythe CDC/National Healthcare Safety Network (NHSN)Surveillance as “a localized or systemic condition result-ing from an adverse reaction to the presence of an infec-tious agent(s) or its toxin(s) [6,7]. There must be noevidence that the infection was present or incubating atthe time of admission to the acute care setting.” The“big four,” which are the 4 most common types, areurinary tract infections (UTI), surgical site infections(SSI), bloodstream infections (BSI), and pneumonia(PNEU) [6,7]. SSIs account for roughly 1/3 of all HAIs,and catheter-associated BSIs, catheter-associated UTIs,and ventilator-associated pneumonias account for theremaining 2/3 [6,7].SSIs are classified into incisional and organ/space, with

specific criteria for each [6,7]. Incisional is sub-classifiedinto superficial incisional, involving only the skin andsubcutaneous tissue, and deep incisional, involving fasciaand muscle. Organ/space SSI involves any part of thebody that was opened or manipulated during the oper-ation, excluding the incision, fascia, and muscle layers.For a more detailed description of each, including signs/symptoms, please refer to CDC/NHSN criteria [6,7].

GoalsThe goal of this review is to impress that this issueshould be paramount to the daily practice of medicine.To that aim, we provide an update and succinct sum-mary of the literature regarding the etiology of HAIs andhighlight some preventive measures that can be success-fully implemented, specifically concerning SSIs. We alsobriefly introduce a novel treatment methodology thatour lab has been developing as a potential avenue tocombat nosocomial SSIs. Lastly, we want to emphasizethe implications of this issue to the healthcare systemand to the individual patient.

Pathophysiology/etiologyThe etiology of HAIs is undeniably multifactorial. How-ever, the source of contamination can often be attributedto the endogenous skin flora of either the patient or hos-pital staff [8-10]. There are two categories of flora: residentand transient [9,11,12]. Resident flora are microorganismsthat normally colonize an individual and live in harmonywith the host, usually providing some benefit or protec-tion [9,11,12]. Conversely, transient flora are microor-ganisms picked up from the environment. They oftendo not survive very long on the host, but are easilytransmissible from one to another or back to the envir-onment [9,11,12].Often referred to as the human “microbiota”, the resi-

dent flora vastly outnumber human host cells by 10–100times and form a commensal community. Over the pastdecade, new sequencing technologies and emerging fieldssuch as metagenomics have enabled researchers to begincharacterizing this intricate, dynamic micro-ecosystemand its implication on host health and disease [12-16]. Itis thought that a disruption or alteration of the complexinteractions among human cells and endogenous microor-ganisms can lead to disease states, such as autoimmune,metabolic, infectious, inflammatory, and even psycho-logical disorders. In the realm of HAIs, studies have sug-gested that the microbiota can act as a physical barrier tocolonization and/or keep the potential virulence of someendogenous microorganisms in check [12-16]. An insultto host homeostasis whether as a consequence of surgeryor another process may in fact disturb the balance of thisdelicate ecosystem, permitting the overgrowth of specificstrains of resident flora with pathogenic potential and/orcolonization of transient flora, transmitted by the environ-ment or by hospital staff [12-16].Some of the most common microorganisms that ac-

count for HAIs include coagulase-negative staphylococci,Staphylococcus aureus, Enteroccocus species, Candida,Escherichia coli, Pseudomonas, and Klebsiella [17]. Thereis a significant percentage of HAIs associated withmultidrug-resistant pathogens (~16%) [17]. The mostcommon includes Methicillin-resistant Staphylococcusaureus (MRSA), accounting for 8%, Vancomycin-resistantEnterococci faecium (VRE), and Carbapenem-resistant P.aeruginosa [17]. About 25-30% of the community isnow colonized by S. aureus and up to 5% are colonizedwith MRSA [18].These microorganisms spread through many routes.

The most common of which includes contact, air, water,and vehicle.• Contact transmission is by direct contact, and per-

haps the most common and easiest way for resident andtransient flora to spread to a susceptible patient. It is alsothe route most easily traced back to healthcare workersand staff. This is often due to improper hand hygiene,














































References





[52-54]

























[67-69]





[72,73]

































[84-87]





[92-95]


[96-99]



















































































































































s13037-014-0042-5.pdf














































References





[52-54]

























[67-69]





[72,73]

































[84-87]





[92-95]


[96-99]



















































































































































s13037-014-0042-5.pdf























[67-69]





[72,73]

































[84-87]





[92-95]


[96-99]



















































































































































s13037-014-0042-5.pdf






















[84-87]





[92-95]


[96-99]



















































































































































s13037-014-0042-5.pdf











































































































































s13037-014-0042-5.pdf

prevencion infecciones sitio quirúrgico

Documents

Transcript of prevencion infecciones sitio quirúrgico